6th International Symposium on Intensive Care and Emergency by A. F. Junod (auth.), Dr. J. L. Vincent (eds.)

By A. F. Junod (auth.), Dr. J. L. Vincent (eds.)

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Additional resources for 6th International Symposium on Intensive Care and Emergency Medicine: Brussels, Belgium, April 15–18, 1986

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There is no question from desitometry that seawater results in hemoconcentration and freshwater hemodilution. These changes occur only with very high volumes of fluid and are not of major clinical importance. In a large series of near-drowned patients who were admitted to the University of Florida hospital, the initial serum concentrations of sodium, chloride, and potassium were virtually indistiguishable whether the drowning occurred in freshwater, saltwater, or brackish water [2]. Also if there are acute changes in electrolyte and blood volume, these tend to be transient and are observed mainly during the first 10 minutes after the onset of submersion.

Little information is available about lung uptake following acute injury in man. However labelled neutrophils exposed to endotoxin are almost entirely sequestrated in the lung following intravenous injection into experimental animals. Lung lavage has become a safe and valuable tool for research into lung injury. Its main application has been to assess inflammation of the lower respiratory tract, in particular to identify the types and numbers of leucocytes present in alveolar liquid. The greatest emphasis has been placed on the leucocyte composition of lavage fluid in patients with chronic interstitial lung disease but recently the technique is playing an important role in the diagnosis of pneumonia in immunosuppressed patients [20].

This results in acute respiratory failure through pulmonary edema. Involvement of polymorphonuclear cells (PMN) as effector cells initiating the vascular injury was proposed by Craddock, Jacob and coworkers [1, 2]. The arguments are based on morphologic observations of the accumulation or sequestration of PMN in the pulmonary vasculature of animal models of ARDS, induced by a veriety of stimuli such as endotoxemia, bacteremia, hemorrhagic shock, cardiopulmonary bypass, complement-activated sera, etc ...

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